相似文献
1
A soluble form of Epstein-Barr virus gH/gL inhibits EBV-induced membrane fusion and does not function in fusion.一种可溶性形式的 Epstein-Barr 病毒 gH/gL 抑制 EBV 诱导的膜融合，并且不在融合中发挥功能。
Virology. 2013 Feb 5;436(1):118-26. doi: 10.1016/j.virol.2012.10.039. Epub 2012 Nov 29.
2
The Cytoplasmic Tail Domain of Epstein-Barr Virus gH Regulates Membrane Fusion Activity through Altering gH Binding to gp42 and Epithelial Cell Attachment.爱泼斯坦-巴尔病毒gH的胞质尾域通过改变gH与gp42的结合及上皮细胞附着来调节膜融合活性。
mBio. 2016 Nov 15;7(6):e01871-16. doi: 10.1128/mBio.01871-16.
3
Binding-site interactions between Epstein-Barr virus fusion proteins gp42 and gH/gL reveal a peptide that inhibits both epithelial and B-cell membrane fusion.爱泼斯坦-巴尔病毒融合蛋白gp42与gH/gL之间的结合位点相互作用揭示了一种可抑制上皮细胞膜融合和B细胞膜融合的肽段。
J Virol. 2007 Sep;81(17):9216-29. doi: 10.1128/JVI.00575-07. Epub 2007 Jun 20.
4
The Epstein-Barr virus (EBV) glycoprotein B cytoplasmic C-terminal tail domain regulates the energy requirement for EBV-induced membrane fusion.爱泼斯坦-巴尔病毒（EBV）糖蛋白B胞质C末端尾域调节EBV诱导膜融合所需的能量。
J Virol. 2014 Oct;88(20):11686-95. doi: 10.1128/JVI.01349-14. Epub 2014 Aug 6.
5
Mapping the N-terminal residues of Epstein-Barr virus gp42 that bind gH/gL by using fluorescence polarization and cell-based fusion assays.利用荧光偏振和基于细胞的融合测定法绘制 Epstein-Barr 病毒 gp42 与 gH/gL 结合的 N 端残基图谱。
J Virol. 2010 Oct;84(19):10375-85. doi: 10.1128/JVI.00381-10. Epub 2010 Jul 28.
6
Membrane anchoring of Epstein-Barr virus gp42 inhibits fusion with B cells even with increased flexibility allowed by engineered spacers.爱泼斯坦-巴尔病毒gp42的膜锚定抑制了与B细胞的融合，即使工程化间隔序列增加了其灵活性。
mBio. 2015 Jan 6;6(1):e02285-14. doi: 10.1128/mBio.02285-14.
7
Epstein-Barr Virus Fusion with Epithelial Cells Triggered by gB Is Restricted by a gL Glycosylation Site.由gB触发的爱泼斯坦-巴尔病毒与上皮细胞的融合受gL糖基化位点限制。
J Virol. 2017 Nov 14;91(23). doi: 10.1128/JVI.01255-17. Print 2017 Dec 1.
8
Soluble Epstein-Barr virus glycoproteins gH, gL, and gp42 form a 1:1:1 stable complex that acts like soluble gp42 in B-cell fusion but not in epithelial cell fusion.可溶性爱泼斯坦-巴尔病毒糖蛋白gH、gL和gp42形成1:1:1的稳定复合物，该复合物在B细胞融合中表现得像可溶性gp42，但在上皮细胞融合中则不然。
J Virol. 2006 Oct;80(19):9444-54. doi: 10.1128/JVI.00572-06.
9
Functional homology of gHs and gLs from EBV-related gamma-herpesviruses for EBV-induced membrane fusion.EBV相关γ-疱疹病毒的gHs和gLs对EBV诱导的膜融合的功能同源性。
Virology. 2007 Aug 15;365(1):157-65. doi: 10.1016/j.virol.2007.03.054. Epub 2007 May 2.
10
The conserved disulfide bond within domain II of Epstein-Barr virus gH has divergent roles in membrane fusion with epithelial cells and B cells.爱泼斯坦-巴尔病毒gH结构域II内保守的二硫键在与上皮细胞和B细胞的膜融合中具有不同作用。
J Virol. 2014 Dec;88(23):13570-9. doi: 10.1128/JVI.02272-14. Epub 2014 Sep 17.
引用本文的文献
1
GB and gH/gL fusion machinery: a promising target for vaccines to prevent Epstein-Barr virus infection.GB 和 gH/gL 融合机制：预防 EBV 感染疫苗的有前景的靶点。
Arch Virol. 2024 Jul 17;169(8):167. doi: 10.1007/s00705-024-06095-3.
2
The structural basis of herpesvirus entry.疱疹病毒进入的结构基础。
Nat Rev Microbiol. 2021 Feb;19(2):110-121. doi: 10.1038/s41579-020-00448-w. Epub 2020 Oct 21.
3
Functional Relevance of the Transmembrane Domain and Cytoplasmic Tail of the Pseudorabies Virus Glycoprotein H for Membrane Fusion.伪狂犬病毒糖蛋白 H 的跨膜域和胞质尾对膜融合的功能相关性。
J Virol. 2018 May 29;92(12). doi: 10.1128/JVI.00376-18. Print 2018 Jun 15.
4
Human MHC-II with Shared Epitope Motifs Are Optimal Epstein-Barr Virus Glycoprotein 42 Ligands-Relation to Rheumatoid Arthritis.人类 MHC-II 共享表位基序是最佳的 Epstein-Barr 病毒糖蛋白 42 配体 - 与类风湿关节炎的关系。
Int J Mol Sci. 2018 Jan 21;19(1):317. doi: 10.3390/ijms19010317.
5
The COMPLEXity in herpesvirus entry.疱疹病毒进入过程中的复杂性。
Curr Opin Virol. 2017 Jun;24:97-104. doi: 10.1016/j.coviro.2017.04.006. Epub 2017 May 21.
6
The Cytoplasmic Tail Domain of Epstein-Barr Virus gH Regulates Membrane Fusion Activity through Altering gH Binding to gp42 and Epithelial Cell Attachment.爱泼斯坦-巴尔病毒gH的胞质尾域通过改变gH与gp42的结合及上皮细胞附着来调节膜融合活性。
mBio. 2016 Nov 15;7(6):e01871-16. doi: 10.1128/mBio.01871-16.
7
Novel Epstein-Barr virus-like particles incorporating gH/gL-EBNA1 or gB-LMP2 induce high neutralizing antibody titers and EBV-specific T-cell responses in immunized mice.包含gH/gL-EBNA1或gB-LMP2的新型爱泼斯坦-巴尔病毒样颗粒在免疫小鼠中诱导出高中和抗体滴度和EBV特异性T细胞反应。
Oncotarget. 2017 Mar 21;8(12):19255-19273. doi: 10.18632/oncotarget.13770.
8
In-cell infection: a novel pathway for Epstein-Barr virus infection mediated by cell-in-cell structures.细胞内感染：一种由细胞中细胞结构介导的爱泼斯坦-巴尔病毒感染新途径。
Cell Res. 2015 Jul;25(7):785-800. doi: 10.1038/cr.2015.50. Epub 2015 Apr 28.
9
Membrane anchoring of Epstein-Barr virus gp42 inhibits fusion with B cells even with increased flexibility allowed by engineered spacers.爱泼斯坦-巴尔病毒gp42的膜锚定抑制了与B细胞的融合，即使工程化间隔序列增加了其灵活性。
mBio. 2015 Jan 6;6(1):e02285-14. doi: 10.1128/mBio.02285-14.
10
Assembly and architecture of the EBV B cell entry triggering complex.EBV B细胞进入触发复合体的组装与结构
PLoS Pathog. 2014 Aug 21;10(8):e1004309. doi: 10.1371/journal.ppat.1004309. eCollection 2014 Aug.
本文引用的文献
1
Herpes simplex virus glycoproteins gH/gL and gB bind Toll-like receptor 2, and soluble gH/gL is sufficient to activate NF-κB.单纯疱疹病毒糖蛋白 gH/gL 和 gB 结合 Toll 样受体 2，可溶性 gH/gL 足以激活 NF-κB。
J Virol. 2012 Jun;86(12):6555-62. doi: 10.1128/JVI.00295-12. Epub 2012 Apr 11.
2
The KGD motif of Epstein-Barr virus gH/gL is bifunctional, orchestrating infection of B cells and epithelial cells.Epstein-Barr 病毒 gH/gL 的 KGD 基序具有双重功能，协调 B 细胞和上皮细胞的感染。
mBio. 2012 Jan 3;3(1). doi: 10.1128/mBio.00290-11. Print 2012.
3
Structure of herpes simplex virus glycoprotein D bound to the human receptor nectin-1.单纯疱疹病毒糖蛋白 D 与人受体 nectin-1 结合的结构。
PLoS Pathog. 2011 Sep;7(9):e1002277. doi: 10.1371/journal.ppat.1002277. Epub 2011 Sep 29.
4
Fusion of Epstein-Barr virus with epithelial cells can be triggered by αvβ5 in addition to αvβ6 and αvβ8, and integrin binding triggers a conformational change in glycoproteins gHgL.除了αvβ6 和 αvβ8，上皮细胞中的 Epstein-Barr 病毒融合还可以被αvβ5 触发，整合素结合触发糖蛋白 gHgL 的构象变化。
J Virol. 2011 Dec;85(24):13214-23. doi: 10.1128/JVI.05580-11. Epub 2011 Sep 28.
5
Human cytomegalovirus glycoprotein gO complexes with gH/gL, promoting interference with viral entry into human fibroblasts but not entry into epithelial cells.人巨细胞病毒糖蛋白 gO 与 gH/gL 复合物，促进干扰病毒进入人成纤维细胞，但不进入上皮细胞。
J Virol. 2011 Nov;85(22):11638-45. doi: 10.1128/JVI.05659-11. Epub 2011 Aug 31.
6
Fusing structure and function: a structural view of the herpesvirus entry machinery.融合结构与功能：疱疹病毒进入机制的结构观
Nat Rev Microbiol. 2011 May;9(5):369-81. doi: 10.1038/nrmicro2548. Epub 2011 Apr 11.
7
Structure of a core fragment of glycoprotein H from pseudorabies virus in complex with antibody.糖蛋白 H 核心片段与抗体复合物的伪狂犬病病毒结构。
Proc Natl Acad Sci U S A. 2010 Dec 28;107(52):22635-40. doi: 10.1073/pnas.1011507107. Epub 2010 Dec 13.
8
Cascade of events governing cell-cell fusion induced by herpes simplex virus glycoproteins gD, gH/gL, and gB.疱疹病毒糖蛋白 gD、gH/gL 和 gB 诱导的细胞融合的级联事件。
J Virol. 2010 Dec;84(23):12292-9. doi: 10.1128/JVI.01700-10. Epub 2010 Sep 22.
9
Crystal structure of the conserved herpesvirus fusion regulator complex gH-gL.疱疹病毒保守融合调节因子复合物 gH-gL 的晶体结构。
Nat Struct Mol Biol. 2010 Jul;17(7):882-8. doi: 10.1038/nsmb.1837. Epub 2010 Jul 4.
10
The Ig-like v-type domain of paired Ig-like type 2 receptor alpha is critical for herpes simplex virus type 1-mediated membrane fusion.配对免疫球蛋白样型 2 受体α的 Ig 样 v 型结构域对于单纯疱疹病毒 1 介导的膜融合至关重要。
J Virol. 2010 Sep;84(17):8664-72. doi: 10.1128/JVI.01039-10. Epub 2010 Jun 23.
Zotero 插件